Common genes and pathways have been discovered that affect individual predisposition to inflammatory diseases of the barrier organs such as asthma, eczema, psoriasis, and the inflammatory bowel diseases (IBDs), Crohn's disease (CD) and ulcerative colitis (UC). 1 The underlying common pathogenetic mechanisms appear to involve a breakdown of the epithelial barrier (in the lungs, skin, or intestine), which leads to increased exposure to environmental stimuli (for instance, bacteria and allergens), and consequent dysregulation of the immune response in predisposed individuals. 2 Some of us have recently shown that genetic variation at the COL29A1 and IL31 loci associates with eczema in different populations. 3,4 COL29A1 is a novel member of the collagen superfamily of extracellular matrix proteins involved in the maintenance of tissue integrity, and is most abundantly expressed in the skin, lung, small intestine, and colon. 3 IL31 has been recently identified as a T cell-derived cytokine with immunomodulatory properties in vitro, 5 and is overexpressed in eczematous skin and in inflamed colonic tissue from both CD and UC patients. 6,7 We reasoned that COL29A1 and IL31 eczema-associated polymorphisms might be relevant to intestinal inflammation, and we therefore tested both genes for association with IBD. We studied 1299 individuals,